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Function of Kidneys
Remove
(a) Nephron
(b) Renal Pyramid with Nephrons
(c) Section of Kidney
Renal Hormone
Regulation
Synthesis and activation of hormones
by the kidney include:
Active form of Vitamin D
Erythropoietin
Renal blood flow regulated by:
Renin-angiotensin aldosterone sy
stem (RAAS)
Valerie Kolmer
2006
A. Definitions
1.Azotemia - elevated blood urea nitrogen (BUN
>28mg/dL) and creatinine (Cr>1.5mg/dL)
2.Uremia - azotemia with symptoms or signs of
renal failure
3.End Stage Renal Disease (ESRD) - uremia
requiring transplantation or dialysis
4.Chronic Renal Failure (CRF) - irreversible kidney
dysfunction with azotemia >3 months
5.Creatinine Clearance (CCr) - the rate of filtration
of creatinine by the kidney (GFR marker)
6.Glomerular Filtration Rate (GFR) - the total rate of
filtration of blood by the kidney
Stage 2
Stage 3
Moderate GFR
GFR 30-59
Stage 4
Severe GFR
GFR 15-29
Stage 5
Kidney failure
Etiology
Diabetic Nephropathy
50K cases of DN ESRD annually
Diabetes most common contributor to ESRD
>30% of ESRD cases attributed to Diabetes
Hypertension
CFR with Hypertension causes 23% of ESRD
annually
Glomerulonephritis: 10%
Polycystic Kidney Disease: 5%
Rapidly progressive glomerulonephritis (vasculitis):
2%
Renal Vascular Disease (i.e., renal artery stenosis)
Medications
Analgesic Nephropathy (progression after many
years)
Pregnancy: high incidence of increased creatitine
and HTN during pregnancy associated with CRF
of GFR
of GFR
Mellitus
Hypertension
Cardiovascular Disease
Obesity
Metabolic Syndrome
Age and Race
Acute Kidney Injury
Malignancy
Proteinuria
Family
history of CKD
Kidney Stones
Infections like Hep C
and HIV
Autoimmune diseases
Nephrotoxics like
NSAIDS
Environmental exposure
(heavy metals and
organic compounds)
Pathophysiology
Susceptibility factors increase the risk for kidney disease but do not directly cause kidney
damage. Susceptibility factors include advanced age, reduced kidney mass and low birth
weight, racial or ethnic minority, family history, low income or education, systemic
inflammation, and dyslipidemia.
Initiation factors initiate kidney damage and can be modified by drug therapy. Initiation
factors include diabetes mellitus, hypertension, autoimmune disease, polycystic kidney
disease, and drug toxicity.
Progression factors hasten decline in kidney function after initiation of kidney damage.
Progression factors include glycemia in diabetics, hypertension, proteinuria, and smoking.
Most progressive nephropathies share a final common pathway to irreversible renal
parenchymal damage and ESRD. Key pathway elements are loss of nephron mass,
glomerular capillary hypertension, and proteinuria.
Pathogenesis
Hyperfiltration Injury
* Final common pathway of glomerular
destruction
* Hypertrophy of remaining nephrons
* Increase glomerular blood flow
* glomerular filtration in surviving
nephrons
* Progressive damage to surviving nephrons
(due to elevated hydrostatic pressure /
toxic effect)
* excretory burden on surviving nephrons
* Sclerosis of nephrons
Normal.
Mild- Generally asymptomatic
Moderate Insufficiency- Generally asymptomatic,
nocturia, HTN,
Mild Anemia
Severe/ Advanced Renal Insufficiency- nocturia, fatigue,
cold intolerance, abnormal taste, anorexia,
hyperphosphatemia, hypoclacemia, hyperkalemia,
metabolic acidosis, worsening anemia
ESRD- Malaise, Lethargy, pruritis, intactable nausea and
vomiting, leg cramps, seizures, worsening parameters,
myoclonus, asterixis Etc
CRF - Manifestations
CRF - Management
Diagnostic
etiology
Treatment of Hypertension and Dyslipidemia
Treatment of Anemia
Treatment of Hyperphosphatemia
Avoidance of Dehydration & Nephrotoxic
agents
Proper Dosing of Drugs
Preparation for Renal Replacement Therapy
CRF - Evaluation
CRF- Evaluation
Serum
electrolytes
Urine spot protein analysis (24 hour no
longer recommended).
ANA, C3, C4
SPEP, UPEP
Kidney Ultrasound
Urine sediment analysis
Biopsy
Evidence of glomerular disease without diabetes
Sudden onset of nephrotic syndrome or
glomerular hematuria
CRF - Management
Diagnostic
etiology
Treatment of Hypertension and Dyslipidemia
Treatment of Anemia
Treatment of Hyperphosphatemia
Avoidance of Dehydration & Nephrotoxic
agents
Proper Dosing of Drugs
Preparation for Renal Replacement Therapy
CKD - Hypertension
Anti-Hypertensive Agents
Single most important measure could be adequate BP control
Target BP <130/80 with minimal proteinuria and BP<125/75
with significant proteinuria (>1g).
ACEIs and ARBs have been demonstrated to slow both
diabetic and non-diabetic renal disease in both experimental
and human studies.
Nondihydropyridine calcium channel blockers are generally used
as second-line antiproteinuric drugs when ACEIs or angiotensin II
receptor blockers are not tolerated.
Decrease the sodium intake to 2.5 g /day
Usually requires more than 2 medications.
Diuretics enhance the antihypertensive and antiproteinuric
effects of other agents.
Hyperkalemia to be monitored with ACEI drugs.
CKD - Dyslipidemia
CKD - Management
Diagnostic
etiology
Treatment of Hypertension and Dyslipidemia
Treatment of Anemia
Treatment of Hyperphosphatemia
Avoidance of Dehydration & Nephrotoxic
agents
Proper Dosing of Drugs
Preparation for Renal Replacement Therapy
CKD - Anemia
Decreased
quality of
life with anemia.
Diagnosis of
exclusion.
Mostly apparent in
the stage 4 and 5 of
CKD.
Due to decrease in
EPO production in
the kidney.
CKD - Anemia
CKD - Management
Diagnostic
etiology
Treatment of Hypertension and Dyslipidemia
Treatment of Anemia
Treatment of Hyperphosphatemia
Avoidance of Dehydration & Nephrotoxic
agents
Proper Dosing of Drugs
Preparation for Renal Replacement Therapy
SECONDARY HYPERPARATHYROIDISM
AND RENAL OSTEODYSTROPHY
CKD - Hyperphosphatemia
Control of Hyperphosphatemia
Due to decreased excretion in urine.
Control of hyperphosphatemia by dietary measures slow progression in
experimental models of CKD.
Hyperphosphatemia leads to pruritus, calcification in synovial membranes,
blood vessels and even cardiac valves.
Therapy includes Phosphorus restriction to 800mg/day and use of
phosphrous binders with food.
Calcium Carbonate (TUMS), Ca-acetate (PHOSLO)
Lanthanum carbonate
sevelamer HCL
Phosphate-binding agents decrease phosphorus absorption from the gut andare
first-line agents for controlling both serum phosphorus and calcium
Concentrations .
METABOLIC ACIDOSIS
CKD - Management
Diagnostic
etiology
Treatment of Hypertension and Dyslipidemia
Treatment of Anemia
Treatment of Hyperphosphatemia
Avoidance of Dehydration & Nephrotoxic
agents
Proper Dosing of Drugs
Preparation for Renal Replacement Therapy
CKD - Nephrotoxics
Avoidance
Agents
of Dehydration/Nephrotoxic
CKD - Management
Diagnostic
etiology
Treatment of Hypertension and Dyslipidemia
Treatment of Anemia
Treatment of Hyperphosphatemia
Avoidance of Dehydration & Nephrotoxic
agents
Proper Dosing of Drugs
Preparation for Renal Replacement Therapy
Dosing of Drugs
Dose
CKD - Management
Diagnostic
etiology
Treatment of Hypertension and Dyslipidemia
Treatment of Anemia
Treatment of Hyperphosphatemia
Avoidance of Dehydration & Nephrotoxic
agents
Proper Dosing of Drugs
Preparation for Renal Replacement Therapy
CKD - RRT
Preparation
Therapy
CKD - RRT
Indications
Indications
(Absolute):
(Relative):
CKD - RRT
Transplantation:
Preemptive transplant
carries both patient
and graft survival
advantage.
Graft survival better
with living donor
kidneys.
Immunosuppresion is
almost always a
must.
CKD - RRT
Transplantation:
(recent or metastatic)
Current infection
Severe extra renal disease
Active use of illicit drugs
CKD - Summary
In